The effect of SSRI use on the clinical presentation of Alzheimer's disease and
  
   Lead Investigator:    Sienna Carpenter
   Institution      :    Boston University Medical Center
   E-Mail           :    scarpen3@bu.edu
   Proposal ID      :    1163



   Proposal Description:
   1. While our understanding of Alzheimer?s Disease (AD) has grown tremendously in the past few decades, we are still in need of an effective treatment.     Currently, researchers are working to find an effective and safe drug treatment to treat Alzheimer?s Disease. Findings suggest that drugs able to decrease the amount of beta Amyloid in the brain should slow down/stop the progression of Alzheimer?s Disease in the brain. Unfortunately, the development of these drugs takes an exorbitant amount of time and resources. Meanwhile, there are millions of individuals and families suffering through the course of Alzheimer?s Disease.    In the late 1990s and early 2000s people started to notice that the cognitive presentation of Alzheimer?s patients would improve with the use of certain SSRIs. SSRIs are generally prescribed to treat depression and anxiety symptoms due to their effects on the serotonergic system. At the time, it was unclear whether this observed benefit in those suffering from Alzheimer?s Disease was caused by reduced anxious and depressive symptoms or if it were because these drugs were doing something else in the brain related to the neuropathology of this neurodegenerative disease. In the past decade, researchers have been attempting to distinguish whether these perceived cognitive benefits are due to a reduction in anxious and depressive symptoms or if SSRIs are slowing down the pathology of Alzheimer?s Disease.    Multiple studies conducted in transgenic AD mice have looked into the changes in the brain that occur when these mice are given SSRIs. The three most commonly studied SSRIs are fluoxetine, paroxetine and citalopram (escitalopram). These have been longitudinal studies aimed at understanding how SSRIs impact AD mice brains. Findings from this research suggests that these drugs prevent apoptosis in neuronal cells, protect neural synapses, and increase expression of the Wnt/B-catenine pathway associated with anti-AD effects. They have also been sho